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the vacuole (Groover et al., 1997). All these observations revealed that one of the most critical steps in PCD is the irreversible disruption of tonoplast. Secondary wall lignification is initiated before the vacuole rupture. It was found recently that brassinosteroid biosynthetic pathway is activated before the tracheary element PCD, and the synthesized brassinosteroids induce PCD and the formation of secondary cell walls (Yamamoto et al., 2001). In animals apoptosis usually involves nuclear shrinkage and fragmentation, cellular shrinkage, DNA fragmentation, membrane budding, formation of apoptotic bodies and digestion by macrophages or adjacent cells (Wyllie et al., 1980). But nuclear shrinkage and fragmentation do not occur in tracheary PCD, no prominent chromatin condensation is established, although the nucleus sometimes exhibits chromatin condensation near the nuclear envelope (Lai and Srivastava, 1976; Groover et al., 1997; Obara et al., 2001). Cellular shrinkage, membrane blebbing and the formation of apoptotic bodies do not occur in tracheary element PCD. No DNA ladder has been detected in differentiating tracheal elements. Therefore the morphological features of tracheary elements PCD are different from those of apoptosis. Rapid nuclear degradation after vacuole ruptures implies the involvement of a highly active nuclease. In cultured Zinnia cells at least seven active RNase bands were detected by gel assay (Thelen and Northcote, 1989). Proteases are also involved in the autolytic processes of tracheary element PCD. Several protease activities have been found associated with tracheary element differentiation in the Zinnia system (Obara and Fukuda, 2003). Extracts from Zinnia cells cultured in tracheary element inductive medium contain cystein protease activity (Minami and Fukuda, 1995; Beers and Freeman, 1997). Serine proteases may also be involved in tracheary element PCD. Serine proteases of 145 kDa and 60 kDa have been detected specifically in differentiating tracheary elements (Beers and Freeman, 1997). Many cell death related hydrolytic enzymes are expressed during the autolysis of tracheary elements. These enzymes may be harmful to the other cells if they leak from dead tracheary cells. Therefore, the vascular tissue may have some system by which harmful extracellular enzymes are detoxified. Apoptosis in senescence Apoptosis in plants 13 Senescence in plants can refer to at least two distinct processes: The aging of various tissues and organs as the whole plant matures and the process of the whole plant death that sometimes occurs after fertilization and called as monocarpic senescence (Nooden, 1988). Senescence is a genetically controlled developmental process, which is internally programmed (Nooden and Guiamet, 1996). Ultrastructural researches showed that some features of senescence resemble to the typical markers of PCD. Orzaez and Granell (1997a) established typical DNA fragmentation during the senescence of unpollinated pistils of Pisum sativum. Apoptotic parameters were detected during the petal senescence by Orzaez and Granell (1997b). Same researchers also reported the control of DNA fragmentation by ethylene in connection with senescence. These results provide direct evidence to support that the natural senescence of the leaves is indeed apoptotic process (Yen and Yang, 1998). Several researches have tried to find out molecular approaches to identifying genes involved in senescence control. Several genes termed senescence associated genes (SAG) that show sequence similarity to cysteine proteases induced early senescence (Hensel et al., 1993; Lohman et al., 1994). These plant proteases are good candidates for cell death initiation genes. It has also been suggested that RNase (Blank and McKeon, 1989) and lipoxygenase (Rouet-Mayer et al., 1992) activities are also might be involved in senescence control, since the activity of these enzymes increases during senescence, but no casual link between these activities and senescence has been established, yet. Early researches for genes induced during senescence were unsuccessful to identify transcription factors associated with senescence. But in the last few years with the use of new and powerful techniques, new senescence-associated genes (SAGs) have been identified. A number of potential transcription factors are now known to be associated with senescence (Yang et al., 2001; Zentgraf and Kolb, 2002). Receptor like protein kinases has been concerned in senescence signaling (Robatzek and Somssich, 2002). It is known that receptor like kinases serve as receivers and transducers of external stimuli, acting through phosphorylation/dephosphorylation cascades that lead to changes in gene expression. The
14 Narcin Palavan-Unsal et al. Figure 2: A summary of the development of tracheal element PCD. As the PCD process progresses tracheal elements accumulate hydrolytic enzymes in the central vacuole. The transport of organic anions (A-) into the vacuole declines. Tracheal elements become highly vacuolated and their nuclei are tightly pressed and flattened. Secondary cell walls become visible, the central vacuoles in tracheal elements collapse, resulting in the release of hydrolytic enzymes. DNA in tracheal elements is rapidly degraded within 10-20 min of the collapse of the vacuole. After several hours, perforations open at one longitudinal end of each tracheal element, and tracheal elements lose their cellular contents (adapted from Obara and Fukuda, 2003). senescence associated kinase receptor gene (SARK) behaves as typical SAG that is induced by senescenceinducing factors (ethylene, jasmonate) and repressed by senescence delaying factors (cytokinin, light). Both transcript and protein appear prior to onset of senescence (Hajouj et al., 2000). Programmed cell death in response to abiotic stress Plant cells and tissues exposed to variety of abiotic stresses that ultimately may result in their death. Abiotic stresses include toxins such as salinity, metals, herbicides and gaseous pollutants, including reactive oxygen species (ROS), as well as water deficit and water logging, high and low temperature and extreme illumination. Plants show adaptations to the stress including mechanisms to tolerate the adverse conditions, to exclude the toxins or to avoid conditions where the stress is extreme. Abiotic stress may also result in stunted growth, followed by death of part or all of the plant. Cell death in abiotic stress may therefore be part of a regulated process to ensure survival. Alternatively, it may be due to the uncontrolled death of cells or tissues killed by unfavorable conditions. PCD may be a part of an adaptive mechanism to survive the stress. Adaptation of plants to environmental conditions such as high light intensity or low humidity often involves covering their surfaces with layer of dead unicellular hairs. These cells are thought to go through PCD resulting in the formation of a protective layer that functions to block high irradiance and trap humidity (Greenberg, 1996). Aerenchyma is the term given to tissues containing gas spaces. It is frequently observed in the roots of wetland species, but may also be formed in some dryland species in unfavorable conditions. It is formed either constitutively or because of abiotic stress, generally originating from water logging. Aerenchyma has been described in two basic types: Lysigenous and
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